USA: National Institutes of Health (NIH) intramural ME/CFS study

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cfsandmore said:
Is it the data from this study?

https://www.s4me.info/threads/characterization-of-post–exertional-malaise-in-patients-with-myalgic-encephalomyelitis-chronic-fatigue-syndrome-2020-nath-et-al.16927/
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Yes. That thread is about the study they did of PEM as a preliminary to the main NIH study, and which I got very cross and wrote to them about because they appeared not to understand PEM, conflating it with the daily fatiguability symptoms pwME experience, and using stupid methodology.

For me this didn't bode well for accurate diagnosis and patient selection for the main study. I hope I'm wrong, but combining that with the small sample size and the known opinions of Wallit before the trial started and his role running the study, I am skeptical they will have discovered anything useful. I fear it may be just stuff about stress hormones or something else irrelevant that is a downstream effect of being sick and under the stress of undergoing so many tests.

I hope I'm wrong and I live long enough to see something useful come out of it.
 
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From the article
"Nath acknowledged that patients want to see results, but when asked if he would consider posting the draft paper as a preprint – a method of sharing research before formal peer review – he balked. He said top medical journals tend to reject papers that have gotten attention as preprints, and he also favors letting peer review run its course before sharing findings."

and yet he is an author on this preprint, Preprint: Neuropathic symptoms with SARS-CoV-2 vaccination, 2022, Safavi, Walitt, Oaklander, Nath et al
 
Andy said:
From the article
"Nath acknowledged that patients want to see results, but when asked if he would consider posting the draft paper as a preprint – a method of sharing research before formal peer review – he balked. He said top medical journals tend to reject papers that have gotten attention as preprints, and he also favors letting peer review run its course before sharing findings."

and yet he is an author on this preprint, Preprint: Neuropathic symptoms with SARS-CoV-2 vaccination, 2022, Safavi, Walitt, Oaklander, Nath et al
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Am just hypothesizing here but.. throughout Covid, scientists used preprints to get information out quickly. Perhaps that is the case here since it’s a vaccine paper. And perhaps bc of the constant controversy surrounding ME, he is taking extra precautions to not open their paper or process up to unwarranted criticisms, and to do things more formally.
 
While this article is mostly about Long Covid, posting it here for this quote, especially the part that I have bolded.

Why Some Stay Sick
Unraveling Long COVID Alongside Other Post-viral Illnesses

"At the National Institute of Neurological Disorders and Stroke (NINDS), Senior Investigator Avindra Nath, who’s known for his work on how infections affect the brain, and his colleague Brian Walitt have repurposed their observational study on myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)—yet another unexplained condition associated with a previous history of infection that looks a lot like PASC. (Results from the ME/CFS study are expected to be published in 2023.)"

https://irp.nih.gov/catalyst/v30i4/why-some-stay-sick
 
Cort Johnson

https://www.healthrising.org/blog/2022/12/09/avindra-nath-chronic-fatigue-long-covid-interview/

Wish that they would submit the draft articles as preprints.

Summary
  • Three years after the pandemic interrupted any attempts to get back to DC and see Avindra Nath I was back. (This time I was on time. (lol)).
  • Nath is finishing up the 5-year (but interrupted) NIH Intramural ME/CFS study which included two week-long stays at the facility, exercise testing, immune testing, brain imaging, etc, etc.
  • The study was truncated by the pandemic but Nath said mounds of data were gathered and the goal of the study – to uncover areas for the NIH to study – was met.
  • The study was so wide-ranging the five different research teams participated and ultimately collaborated with each. One large paper is almost done and Nath expects many smaller papers to come out of it. He said the study had sparked “huge interest” and called the results “fascinating”.
  • Nath, an immunologist, said he found evidence of immune activation but could not say whether was driving the disease, was an add-on effect, or if it might be protective.
  • His COVID-19 brain autopsy work, though, suggested that antibodies were attracting immune cells and platelets to the endothelial cells lining the blood vessels and causing blood vessels leaks which were being mopped up by macrophages.
  • The trouble is that macrophages are not supposed to be in the brain and once they’re there they behave like unwanted guests: i.e. they stick around.
  • If macrophages are the issue – and some other studies suggest they might be – Nath noted that a variety of immunotherapies (IVIG; anti-TNF-a, IL-1, IL-6, or JakStat inhibitors) could be helpful. These types of drugs are already being discussed with regard to long COVID in conferences.
  • Recent strains of the virus are less virulent but more immune evasive and stick around longer in the body. In the long term it’s possible they cause more damage including things like long COVID.
  • Nath called diseases like ME/CFS, long COVID, fibromyalgia, POTS, post-Lyme Syndrome, Gulf War Illness, and Sick Building Syndrome the “mysteries of medicine” and believes that “if you solve one – you’ll solve them all.”
  • He proposed that “the best way to get at any one of them is to pick one and throw everything at it and solve it. Don’t jump around studying a little bit of this one and a little bit of that one – pick one and dig into it. You’ll probably find that what you found there is applicable to all these other diseases.”
  • Nath believes the long COVID field is exploding and that over the next year we’re going to learn a lot.
  • He’s not concerned about the ability of the ME/CFS field to integrate the findings that are sure to come from long COVID into it stating “It’s all going to get integrated….Even if you wanted to, you couldn’t separate them. There’s no reason to fear.”
 
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"I asked Nath how the early end of the ME/CFS study had affected it?

Nath replied that the sample size was smaller than what he would have wanted but that they’d studied everyone extensively and collected a lot of data on them. The studies were probably going to get critiqued in the journals because of their small sample size, but the goal of the project – to find further avenues for research – was accomplished."

Has it though? Will the NIH justify spending a lot more money in the future if the study is statistically weak? The cynical part of me thinks that someone put pressure to stop the study early as they were afraid of it's potential to change the status quo. Saying they had to stop because of the pandemic and never finish a study makes no sense to me, has it happened in any other illness? I think not.
 
Jaybee00 said:
post-Lyme Syndrome
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Yeah, so that's not even a thing, not even in Bethesda at the NIH. It's not a thing anywhere.

Jaybee00 said:
  • Nath called diseases like ME/CFS, long COVID, fibromyalgia, POTS, post-Lyme Syndrome, Gulf War Illness, and Sick Building Syndrome the “mysteries of medicine” and believes that “if you solve one – you’ll solve them all.”
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How optimistic yet unlikely it would play out so neatly. I would find it unsettling if he actually used this wording.
 
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Jaybee00 said:
He proposed that “the best way to get at any one of them is to pick one and throw everything at it and solve it. Don’t jump around studying a little bit of this one and a little bit of that one – pick one and dig into it. You’ll probably find that what you found there is applicable to all these other diseases.”
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Wow, what a coincidence, that this is what we've been asking for decades. Normal, seeing how obvious it is. But we kept being told it's stupid to think that since it wouldn't accomplish anything. It's a good thing much of this will coincide with AI making it possible to just dump decades of old documents and understand it all, putting all the blame where it deserves.
 
Jaybee00 said:
  • post-Lyme Syndrome, Gulf War Illness, and Sick Building Syndrome the “mysteries of medicine” and believes that “if you solve one – you’ll solve them all.”
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What rubs me the wrong way here is that, perhaps inadvertantly, he's made a statement he cannot factually demonstrate yet. We may all of us in each of these diseases, have compromised immune systems which generate our symptoms. This may be what they ultimately prove.

But I can tell you they have not done that yet with Lyme. Period. They have not shown that all those people with chronic Lyme who have labs proving they had Lyme, and received treatment, no longer have any viable spirochetes. As far as we know, all those hundreds of thousands of Lyme patients, even after months of abx, still may have Lyme.

So to throw about "post-Lyme Syndrome" seems premature at the very least, and arguably political, but at the worst, he's let slip a strategy that may not be good for at least a subset of the diseases he listed in that interview.
 
--- pretty much what others are saying.

I'd be a bit worried if they focused on a form of Long Covid which was e.g. due to (blood) circulation issues and had no relationship to any of the other diseases mentioned.

I'm guessing that there's a proportion of Long Covid that is the same as ME/CFS, and maybe even ME/CFS & Lyme overlap entirely. However, if there's too narrow a focus, on one sub-group of Long Covid, then there may be little/no benefit for ME/CFS and/or Lyme.

Also, I can't understand why there are no plans/demands from patient groups for GWAS studies --- basically if everyone tests their pet theory then you could spend all of the money and end up with little or nothing --- GWAS might point the finger at the right pathway --- something that isn't a pet theory of any scientist who succeeds in getting funded!

I think I may have emailed Nath suggesting GWAS.
 
FMMM1 said:
--- pretty much what others are saying.
Also, I can't understand why there are no plans/demands from patient groups for GWAS studies --- basically if everyone tests their pet theory then you could spend all of the money and end up with little or nothing --- GWAS might point the finger at the right pathway --- something that isn't a pet theory of any scientist who succeeds in getting funded!
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I haven't pushed for a GWAS because DecodeME exists. Hope I can trust the British scientists this time ;). But seriously, we need a GWAS for long Covid. Design would have to be careful because LC isn't one disease or even one syndrome--there are multiple clusters of symptoms.
 
RedFox said:
I haven't pushed for a GWAS because DecodeME exists. Hope I can trust the British scientists this time ;). But seriously, we need a GWAS for long Covid. Design would have to be careful because LC isn't one disease or even one syndrome--there are multiple clusters of symptoms.
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Yea, think we need one (GWAS) for Lyme (PTLS) too.

Yea, I thought the fact that Chris Ponting was doing a GWAS study would be a factor, but I suspect there's benefit in doing several ME/CFS GWAS studies and combining the data.
 
Hubris said:
IMO the fact that the NIH is not doing GWAS for long covid shows they are not taking it seriously. It is such an obvious thing to do and the money is literally there.
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Maybe put that comment to NIH --- not sure how --- I responded to Cort's article --- I wouldn't expect NNIH to read those but ----

Nath mentioned the identification of rare genetic mutations in Alzheimer's i.e. as a potential route to discover mechanism for ME/CFS
Perhaps the study Nath referred to?:

https://jamanetwork.com/journals/jamaneurology/article-abstract/2793004
 
Hubris said:
IMO the fact that the NIH is not doing GWAS for long covid shows they are not taking it seriously. It is such an obvious thing to do and the money is literally there.
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I can't really see how a GWAS could be relevant without far tighter definition of what is meant by Long COVID, there are multiple post-acute sequelae of SARS-CoV-2 infection (PASC) which appear in multiple patient clusters, for a GWAS to make any sense clear and consistent real world cluster typing would need to be demonstrated.
 
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